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In contrast to the decline in mortality from many non-infectious, chronic diseases in the UK, death from liver disease has increased exponentially in men and women over the past 40 years. This is primarily because of the over consumption of alcohol, but also the increased prevalence of obesity, which is linked to early pathology through the accumulation of liver fat. Supra-physiological intakes of fructose-containing sugar can produce acute, adverse effects on lipid metabolism, and deliver excess energy that increases bodyweight and the deposition of fat in sites other than adipose tissue, including the liver. This review addresses the variable metabolic origins of liver fat, and the key importance of postprandial lipid metabolism in this respect. The effects of supra-physiological intakes of sugar are also considered in context of the real world and established threshold for the adverse effects of sugar on cardio-metabolic risk factors. The review concludes that while the average intake of sugar in the UK falls well below this critical threshold, intakes in subgroups of adults, and especially adolescents, may be cause for concern. There is also evidence to suggest that raised liver fat, acquired, in part, through an impaired removal of postprandial lipaemia, can increase sensitivity to the adverse effects of sugar at all ages.

The objective of the present study was to determine the glycaemic index (GI) and glycaemic load (GL) values of standard portion sizes of Southeast Asian traditional foods. A total of fifteen popular Southeast Asian foods were evaluated. Of these foods, three were soft drinks, while the other twelve were solid foods commonly consumed in this region. In total, forty-seven healthy participants (eighteen males and twenty-nine females) volunteered to consume either glucose at least twice or one of the fifteen test foods after a 10-12 h overnight fast. Blood glucose concentrations were analysed before consumption of the test food, and 15, 30, 45, 60, 90 and 120 min after food consumption, using capillary blood samples. The GI value of each test food was calculated by expressing the incremental area under the blood glucose response curve (IAUC) value of the test food as a percentage of each participant's average IAUC value, with glucose as the reference food. Among the fifteen foods tested, six belonged to low-GI foods (Ice Green Tea, Beehoon, Pandan Waffle, Curry Puff, Youtiao and Kaya Butter Toast), three belonged to medium-GI foods (Barley Drink, Char Siew Pau and Nasi Lemak), and the other six belonged to high-GI foods (Ice Lemon Tea, Chinese Carrot Cake, Chinese Yam Cake, Chee Cheong Fun, Lo Mai Gai and Pink Rice Cake). The GI and GL values of these traditional foods provide valuable information to consumers, researchers and dietitians on the optimal food choice for glycaemic control. Moreover, our dataset provides GI values of fifteen foods that were not previously tested extensively, and it presents values of foods commonly consumed in Southeast Asia.

To investigate whether obese women can compensate for sucrose added to the diet when it is given blind, rather than gaining weight or exhibiting dysfunctional regulation of intake, in the present study, forty-one healthy obese (BMI 30-35 kg/m²) women (age 20-50 years), not currently dieting, were randomly assigned to consume sucrose (n 20) or aspartame (n 21) drinks over 4 weeks in a parallel single-blind design. Over the 4 weeks, one group consumed 4 × 250 ml sucrose drinks (total 1800 kJ/d) and the other group consumed 4 × 250 ml aspartame drinks. During the baseline week and experimental weeks, body weight and other biometric data were measured and steps per day, food intake using 7 d unweighed food diaries, and mood using ten- or seven-point Likert scales four times a day were recorded. At the end of the experiment, the participants weighed 1·72 (SE 0·47) kg less than the value predicted by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) model; the predicted body weight accounted for 94·3% of the variance in the observed body weight and experimental group accounted for a further 1·1% of the variance in the observed body weight, showing that women consuming sucrose drinks gained significantly less weight than predicted. The reported daily energy intake did not increase significantly, and sucrose supplements significantly reduced the reported voluntary sugar, starch and fat intake compared with aspartame. There were no effects on appetite or mood. Over 4 weeks, as part of everyday eating, sucrose given blind in soft drinks was partially compensated for by obese women, as in previous experiments with healthy and overweight participants.

Research with laboratory species suggests that meals can be terminated by peripheral signals carried to brain feeding centres via hepatic vagal afferents, and that these signals are affected by oxidation of fuels. Pre-gastric fermentation in ruminants greatly alters fuels, allowing mechanisms conserved across species to be studied with different types and temporal absorption of fuels. These fuels include SCFA, glucose, lactate, amino acids and long-chain fatty acid (FA) isomers, all of which are absorbed and metabolised by different tissues at different rates. Propionate is produced by rumen microbes, absorbed within the timeframe of meals, and quickly cleared by the liver. Its hypophagic effects are variable, likely due to its fate; propionate is utilised for gluconeogenesis or oxidised and also stimulates oxidation of acetyl-CoA by anapleurosis. In contrast, acetate has little effect on food intake, likely because its uptake by the ruminant liver is negligible. Glucose is hypophagic in non-ruminants but not ruminants and unlike non-ruminant species, uptake of glucose by ruminant liver is negligible, consistent with the differences in hypophagic effects between them. Inhibition of FA oxidation increases food intake, whereas promotion of FA oxidation suppresses food intake. Hypophagic effects of fuel oxidation also vary with changes in metabolic state. The objective of this paper is to compare the type and utilisation of fuels and their effects on feeding across species. We believe that the hepatic oxidation theory allows insight into mechanisms controlling feeding behaviour that can be used to formulate diets to optimise energy balance in multiple species.

Berries are often consumed with sucrose. They are also rich sources of polyphenols which may modulate glycaemia after carbohydrate ingestion. The present study investigated the postprandial glucose, insulin and glucagon-like peptide 1 (GLP-1) responses to sucrose ingested with berries, in comparison with a similar sucrose load without berries. A total of twelve healthy subjects were recruited to a randomised, single-blind, placebo-controlled crossover study. They participated in two meal tests on separate days. The berry meal was a purée (150 g) made of bilberries, blackcurrants, cranberries and strawberries with 35 g sucrose. The control meal included the same amount of sucrose and available carbohydrates in water. Fingertip capillary and venous blood samples were taken at baseline and at 15, 30, 45, 60, 90 and 120 min after starting to eat the meal. Glucose, insulin and GLP-1 concentrations were determined from the venous samples, and glucose also from the capillary samples. Compared to the control meal, ingestion of the berry meal resulted in lower capillary and venous plasma glucose and serum insulin concentrations at 15 min (P = 0·021, P < 0·007 and P = 0·028, respectively), in higher concentrations at 90 min (P = 0·028, P = 0·021 and P = 0·042, respectively), and in a modest effect on the GLP-1 response (P = 0·05). It also reduced the maximum increases of capillary and venous glucose and insulin concentrations (P = 0·009, P = 0·011 and P = 0·005, respectively), and improved the glycaemic profile (P < 0·001 and P = 0·003 for capillary and venous samples, respectively). These results suggest that the glycaemic control after ingestion of sucrose can be improved by simultaneous consumption of berries.

In healthy older subjects, the glycaemic response to carbohydrate-containing meals is dependent on gastric emptying and intestinal absorption; when the latter is slowed, the magnitude of the rise in glucose is attenuated. The oligosaccharide α-cyclodextrin has been reported to diminish the glycaemic response to starch in young adults; this effect has been attributed to the inhibition of pancreatic amylase. We examined the effects of α-cyclodextrin on gastric emptying of, and the glycaemic and insulinaemic responses to, oral sucrose in healthy older subjects; as sucrose is hydrolysed by intestinal disaccharides, any effect(s) of α-cyclodextrin would not be attributable to amylase inhibition. A total of ten subjects (seven males and three females, age 68-76 years) were studied on 2 d. Gastric emptying, blood glucose and serum insulin were measured after ingestion of a 300 ml drink containing 100 g sucrose, labelled with (99m)Tc-sulphur colloid, with or without 10 g α-cyclodextrin. Gastric emptying was slowed slightly by α-cyclodextrin; this effect was evident between 135 and 195 min and was associated with a slight increase (P < 0·05) in distal stomach retention. After α-cyclodextrin, blood glucose was slightly less (P < 0·05) at 60 min, and serum insulin was less (P < 0·0005) at 90 and 120 min. There was no difference in the incremental areas under the curve (iAUC) for blood glucose, but there was a trend for the iAUC for serum insulin to be lower (P = 0·09) after α-cyclodextrin. We conclude that in a dose of 10 g, α-cyclodextrin has modest effects to slow gastric emptying of, and modify the glycaemic and insulinaemic responses to, oral sucrose, probably due to delayed intestinal carbohydrate absorption.

We evaluated the absorption and metabolism of palatinose in rats by the carbohydrate load test and the 13C- and H2-breath tests. We compared the results of these tests with those of sucrose, since sucrose is an isomer of palatinose and generally known to be degraded and absorbed from the small intestine. In the carbohydrate load test, blood glucose and plasma insulin levels after oral administration of palatinose rose more gradually and reached a maximum that was lower than that after sucrose administration. In the 13C-breath test, rats were orally administrated [1-13C]sucrose or [1-13C]palatinose and housed in a chamber. The expired air in the chamber was collected, and the level of 13CO2 in the expired air was measured at appropriate intervals for 360 min. The value of time taken to reach the maximum concentration for expired 13CO2 from [1-13Cglucose] ([1-13Cglc]) and [1-13Cfructose] ([1-13Cfru]) palatinose was significantly longer than that from [1-13Cglc] and [1-13Cfru]sucrose, respectively. The value of area under the curve (AUC) for [1-13Cglc]palatinose was larger than that for [1-13Cglc]sucrose, but AUC for [1-13Cfru] showed no difference between palatinose and sucrose. In the H2-breath test, the concentration of H2 in the expired air was measured for 420 min. H2 was hardly detected with both palatinose and sucrose and no significant difference was observed between the two groups. These results suggest that palatinose is utilised in vivo at a rate equal to that of sucrose.

Ruminant farming is an important component of the human food chain. Ruminants can use offtake from land unsuitable for cereal crop cultivation via interaction with the diverse microbial population in their rumens. The rumen is a continuous flow fermenter for the digestion of ligno-cellulose, with microbial protein and fermentation end-products incorporated by the animal directly or during post-ruminal digestion. However, ruminal fermentation is inefficient in capturing the nutrient resource presented, resulting in environmental pollution and generation of greenhouse gases. Methane is generated as a consequence of ruminal fermentation and poor retention of ingested forage nitrogen causes nitrogenous pollution of water and land and contributes to the generation of nitrous oxide. One possible cause is the imbalanced provision of dietary substrates to the rumen micro-organisms. Deamination of amino acids by ammonia-producing bacteria liberates ammonia which can be assimilated by the rumen bacteria and used for microbial protein synthesis. However, when carbohydrate is limiting, microbial growth is slow, meaning low demand for ammonia for microbial protein synthesis and excretion of the excess. Protein utilisation can therefore be improved by increasing the availability of readily fermentable sugars in forage or by making protein unavailable for proteolysis through complexing with plant secondary products. Alternatively, realisation that grazing cattle ingest living cells has led to the discovery that plant cells undergo endogenous, stress-mediated protein degradation due to the exposure to rumen conditions. This presents the opportunity to decrease the environmental impact of livestock farming by using decreased proteolysis as a selection tool for the development of improved pasture grass varieties.

Na+/glucose co-transporter 1 (SGLT1) transports dietary sugars from the lumen of the intestine into enterocytes. Regulation of this protein is essential for the provision of glucose to the body and, thus, is important for maintenance of glucose homeostasis. We have assessed expression of SGLT1 at mRNA, protein and functional levels in the intestinal tissue of 28 d old piglets weaned onto isoenergetic diets with differing concentrations of digestible carbohydrate (CHO). We show that expression of SGLT1 remains constant when piglets are fed up to 40 % CHO-containing diets. However, there is a significant increase in SGLT1 expression when the CHO content of the diet is>50 %. Morphometric analyses indicate that the increased expression is not due to a trophic effect. It has been proposed that in rat intestine, in response to a high-CHO diet, GLUT2 (the classical basolateral membrane monosaccharide transporter) is translocated to the luminal membrane of enterocytes to absorb excess dietary glucose. We show, using immunohistochemistry and Western blotting with antibodies raised to amino acids in different epitopes of GLUT2, that under all dietary conditions, low to high CHO, GLUT2 is expressed on the basolateral membrane of pig enterocytes. Furthermore, functional studies indicate that there is no uptake of 2-deoxy-D-glucopyranoside, a specific substrate of Na+-independent glucose transporters into brush-border membrane vesicles isolated from the intestines of piglets either maintained on low- or high-CHO diets. Thus, SGLT1 is the major route for absorption of dietary sugars across the luminal membrane of swine enterocytes.

Practical values to guide food choices for control of postprandial glycaemia need to refer to entire foods in amounts customarily consumed. We tested an in vitro method for determining the relative glycaemic impact (RGI) of customarily consumed portions of foods. Sugars released during in vitro pancreatic digestion of eighty-three foods were measured as glucose equivalents (GE) per gram of food, adjusted by the glycaemic indexes of the sugars to obtain glycaemic GE (GGE) per gram and multiplied by food portion weight to obtain the GGE contribution of the food portion, its RGI. The results were compared with clinical GGE values from subjects who consumed the same food amounts. In vitro and in vivo GGE values were significantly correlated, but the slope of the regression equation was significantly less than one, meaning in vitro GGE values overestimated in vivo GGE values. Bland-Altman method comparison showed the in vitro-in vivo disparity to increase as mean GGE increased, suggesting the need to allow for different rates of homeostatic blood glucose disposal (GD) due to different GGE doses in the customarily consumed food portions. After GD correction, Bland-Altman method comparison showed that the bias in predicting in vivo GGE values from in vitro GGE values was almost completely removed (y = 0.071x - 0.89; R2 0.01). We conclude that in vitro food values for use in managing the glycaemic impact of customarily consumed food quantities require correction for blood GD that is dependent on the GGE content of the food portions involved.

There is increasing concern that high intakes of added sugars might compromise intakes of micronutrients. The objectives of this systematic review were (1) to determine whether dietary added sugar intake was associated with micronutrient intakes, and if so, whether there was evidence of micronutrient dilution as a result of higher dietary added sugar intake and (2) if micronutrient dilution was present, to determine whether there was sufficiently robust evidence to support a threshold effect above which there was a significant decline in micronutrient intake or status relative to the recommended intakes. A systematic computerised literature search was undertaken, limited to studies written in English published from 1980 onwards and further studies identified through hand searching papers. Fifteen studies that assessed associations between intakes of added sugars or non-milk extrinsic sugars and micronutrients were included. Overall, there are insufficient data and inconsistency between studies in relationships between added sugars and micronutrient intakes, with no clear evidence of micronutrient dilution or a threshold for a quantitative amount of added sugar intake for any of the micronutrients investigated. The current evidence base is considerably constrained by methodological issues. Further research is required to determine which food products high in added sugars might adversely affect micronutrient intakes by displacing other food items from the diet. Analyses should take into account the magnitude of any observed associations to determine their true biological significance.

The elevation of blood lipid concentrations in response to the consumption of low-fat high-carbohydrate diets is known as carbohydrate-induced hypertriacylglycerolaemia (HPTG). An understanding of the mechanisms involved in the interaction between carbohydrates and plasma lipids may help determine whether carbohydrate-induced HPTG would increase cardiovascular risk. There is growing evidence to suggest that the sugar component of the diet may be largely responsible, rather than the total carbohydrate. In most studies designed to investigate the mechanisms of carbohydrate-induced HPTG, the amounts and types of sugars and starches used in the diets are not specified. Findings have been mixed and inconsistent. It is proposed that the elucidation of mechanisms from current studies could have been confounded by the different ways in which sugars are metabolized in the body. At present, there are few studies that have evaluated the independent effects of dietary sugars. Interest has been focused on de novo lipogenesis (DNL), as it has recently been found to be positively correlated with increases in fasting TAG levels produced on high-carbohydrate diets, indicating that DNL may contribute to carbohydrate-induced HPTG. DNL has been found to be determined by starch:sugar in a high-carbohydrate diet and affected by different types of sugars. The presence of DNL in adipose tissue is supported by emerging gene-expression studies in human subjects. In the wake of rising intakes of sugars, further research is needed to investigate the mechanisms associated with different sugars, so that appropriate therapeutic strategies can be adopted.